Arterial hypertension is one of the most pervasive health problems in our society today. It is now accepted that the etiology is multifactorial, even if one cause is found to be primarily responsible. Despite tremendous progress in diagnostic methods, essential hypertension, i.e., hypertension in which the initial cause for the development is unknown, consititutes over 90% of cases. Clinical and laboratory evidence for neurogenic involvement in the development of essential hypertension has grown in this decade, but the exact mechanisms involved are still not fully understood. The objective of this research is to continue to study, in an experimental model, the mechanisms responsible for the development of neurogenic hypertension and its possible reversibility. The model is a simulation of a naturally occurring situation in which there is compression of nervous elements in the region of the brainstem by aberrant or ectatic branches of normal arteries. This mechanism was suggested by clinical cases of patients with arterial hypertension who at surgery were observed to have compression on this area by arterial loops. Surgical microvascular decompression was successful in reducing the high blood pressure. The key to this model is the implantation in baboons of a self-contained double balloon device which applies pulsatile pressure upon the entry zone of the IXth and Xth cranial nerves and on the ventrolateral medulla on the left side. The data that we have obtained from the first 2 years work suggest that hypertension develops gradually in response to the pulsatile pressure after 3 to 7 days. This phenomenon is reversible when the stimulus is discontinued. The initial hemodynamic change may involve increases in cardiac output and stroke volume followed by increasing peripheral resistance. Baroreflex sensitivity did not decrease with the development of hypertension. Chronic implantation of the deflated double ballon device for as long as one year does not cause hypertension. Chronic monitoring of cardiac output, heart rate, central blood pressure and ECG will be achieved in the totally unrestrained animal by means of implanted radiotelemetry. The observation of hemodynamic changes will be complemented by study of the baroreflexes and humoral factors. The assimilation of all this data from animals studied for one-year period should lead to an improved understanding of the mechanisms involved in the pathophysiology of neurogenic hypertension.